This is a continued study on the action of calcitonin on phosphate metabolism. It is based on the postulate that most, if not all, physiological changes produced by this hormone are the result of phosphate movement into and out cells. Calcitonin causes the rapid movement of phosphate out of blood, and a major project is to determine where this phosphate goes. The role of bone and kidney are becoming clearer, but as yet we have not determined if other soft tissues are involved. A second project is to compare its action on the kidney with that of other hormones such as parathyroid hormone and glucagon which are also known to act by increasing the activity of adenyl cyclase. This will be studied in EHDP-treated rats. The third study is a cooperative study with Dr. J. L. Matthews (Baylor College of Dentistry, Dallas) in a project which is helping us demonstrate that the hypocalcemic action of calcitonin is probably the result of phosphate movement through and out of specific bone cells. For our last project in this group we are continuing to design experiments in which the hypocalcemic action of calcitonin is abolished while its action on phosphate is at least in part maintained.